Retina Zarieh Dawn L. Novela

Medicine 2

Retina

Layers of Retina1. Pigment epithelium• Derived from outer layer

of optic cup• Composed of single layer

of polygonal cells • Source of metabolic

enzymes, as well as vit.A• Phagocytosis of

degenerated fragments of outer segment

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Layers of Retina1. Pigment epithelium• It prevents light reflection

throughout the eyeball• w/o it, light rays would be

reflected in all directions within the eyeball and would diffuse lighting of retina

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Layers of Retina2. Rods and Cones

(photoreceptors)• Outer segment

– Contains light sensitive photochemicals converting light energy into chemical energy nerve impulse

• Inner segment– Connected to outer

segment by constriction containing cilia (w/c transmits impulses)

– Mitochondria: amplifies weak impulses

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Layers of Retina3. External limiting

membrane• Fenestrated membrane

composed of terminal bars

• Formed by junctional attachment bw membrane of Muller’s cells and inner segment of photoreceptors

3

Layers of Retina4. Outer nuclear layer• Composed of nuclei of

photoreceptors

5. Outer plexiform layer• Composed of axons of

photoreceptors and dendrites of bipolar cells

6. Inner nuclear layer• Composed of nuclei of

several cells (bipolar, Muller, horizontal and amacrine cells)

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6

Layers of Retina7. Inner plexiform layer• Composed of axons of

bipolar cells and dendrites of ganglion cells

8. Ganglion cell layer• Composed of ganglion

cells

9. Nerve fiber layer• Composed of axons of

ganglion cells wc converge toward posterior pole of eye forming optic nerve

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Layers of Retina10. Inner plexiform layer• The cuticular derivative of

Muller’s cells • Serves to delineate the

retina from overlying vitreous

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• Blood supply– Central retinal artery and vein (wc enters the

eye thru optic disk)• As retinal arteries enter the eye, it loses it

internal elastic lamina and the medial muscular coat becomes incomplete.

• The neurosensory retina has no sensory supply – Thus disorders of retina are painless

• 2 capillary networks in retina– In nerve fiber layer and inner nuclear layer

Physiology and Biochemistry of retina• Rods

– func at low level illumination or night vision (scotopic vision)

– peripheral vision– 500x more photosensitive than cones

• Cones– func at high level illumination or daytime vision

(photopic vision) – Central vision– 3 typers: Blue, Green, and Red cones

Physiology and Biochemistry of retina• Fovea centralis

– Center of acute vision (point at which visual perception is sharpest)

– Contains only cones (each with its own neural supply)– Light stimuli in this region can directly act on the sensory

cells because bipolar cells and ganglion cells are displaced peripherally.

• Retina is dependent on constant supply of glucose for its metabolism

• Muller cells– Storehouse of glucose in the form of glycogen

Symptomatology• Principal symptom: visual disturbance Visual blurring

If macula is involved (central serous retinopathy, macular degeneration) – central vision is affected

If extramacular (pigmentary degeneration) – peripheral vision

Photopsia Seeing flashes of light Caused by the fact that any stimulus on eye results in

only one retinal response, that is seeing light May be experienced in retinal and vitreous detachment

Symptomatology Sector visual field defect

Actual loss of part of field of vision or Sensation of curtain or fog covering the involved portion

of field vision Condi: partial retinal defect, branch occlusion on retinal

vessels, and large retinal hemorrhage Disturbance of image size or shape

Metamophopsia: distorted image Micropsia: small image Macropsia: large image Main cause – disturbance in alignment and position of

visual cells

Central retinal artery occlusion (CRAO)• Definition: Retinal infarction due to occlusion of an

artery in the lamina cribrosa or a branch retinal artery occlusion.

• Epidemiology. CRAO occur less often than vein occlusions.

• Common symptom– Blurring or complete loss of vision– Impairment of central vision

Vascular Disturbance

CRAO

• in ophthalmoscope constricted retinal arteries pale optic disk rest of the eye ground is white (due to

coagulation necrosis) cherry red spot“box car” appearance - uninterrupted blood

stream

CRAO

Central retinal artery occlusion (CRAO)• Tx:• Ocular massage, medications that reduce intraocular

pressure, or paracentesis are applied in an attempt to drain the embolus in a peripheral retinal vessel.

• Calcium antagonists or hemodilution are applied in an attempt to improve vascular supply.

• Work-up to identify the source of the embolus is important in order to treat the underlying disease and prevent another embolization (such as stroke).

Vascular Disturbance

Central retinal vein occlusion (CRVO)• Definition: Vein occlusion occurs as a result of

circulatory dysfunction in the central vein or one of its branches.

• Epidemiology. CRVO is the second most frequent vascular retinal disorder after diabetic retinopathy.

• Etiology. Frequently due to local thrombosis at sites where sclerotic arteries compress the veins.

• Common symptom: rapid loss of vision (but not as instant nor complete as CRAO)

Vascular Disturbance

CRVO

• in ophthalmoscope retinal engorgement retinal hemorrhage“hotdog and catsup” appearanceDisk is hyperemic with blurring of the margin

Central retinal vein occlusion (CRVO)• Common complication: Glaucoma

– Occurs 3 mos after onset– Shows neurovascularization of iris surface (rubeosis

iridis) w/ occasional vitreous hemorrhage

• Treatment– In acute stage, hematocrit should be reduced to 35–38%

by hemodilution. – The underlying disorders have to be treated. – Laser treatment is performed in ischemic occlusion that

progresses to neovascularization or rubeosis iridis.

Vascular Disturbance

Hypertensive retinopathy• Definition: Arterial changes in hpn are primarily

caused by vasospasm• Pathogenesis.

– High bp can cause breakdown of the blood–retina barrier or obliteration of capillaries.

– This results in intraretinal bleeding, cotton- wool spots, retinal edema, or swelling of the optic disc.

• Symptoms. – headache or eye pain dt high bp– Impaired vision or loss of visual acuity only occurs in

stage III or IV hypertensive vascular changes.

Retinopathy

Hypertensive retinopathy

Retinopathy

High degree of narrowing

Reduced flow to retina

Anorexia

Incd capillary permeability

Serum or whole blood leaks out into tissue

Retinal edema, exudates or

hemorrhage results

• Severe edema may involve the optic disk → papilledema/chocked disk

• Absorption of edema fluid may leave protein residues → form yellow spots “hard exudate”

• At region of macula, residues are arranged in the form of fan → “macular star”

• Hemorrhage located in nerve fiber layer → “striate or flame-shaped appearance”

• Marked constriction of terminal arterioles may produce zone of infarcts → “cotton wool” patches

Hypertensive retinopathy

Retinopathy

Hypertensive retinopathy

Hypertensive retinopathy

Arteriosclerotic retinopathy• Definition: Arterial changes in hpn as a result of

thickening of the wall of the arteriole.• Commonly seen in atherosclerosis and arteriole

sclerosis• Atherosclerosis.

– Whitish plaques of lipid deposits seen in wall of retinal a.– Lipoidal infiltration as white streak at side of blood

column (“pipestem sheathing”)

Retinopathy

Arteriosclerotic retinopathy• Arteriole sclerosis. 1. Change in median arterioles light streak

Median streak is produced by light reflexed from cylindrical blood column of artery

In thickening and hyalinization of medial coat, MS widens

“copper-wire artery” – when MS completely covers entire blood column

“silver-wire artery” – when sclerosis reaches the advance stage (wc reflects back all the light falling on its surface

Retinopathy

Arteriosclerotic retinopathy• Arteriole sclerosis. 1. Atrio-venous crossing changes

Concealment of vein (Gunn’s sign) Tapering of veins – dt extension of arteriosclerotic

changes Depression of vein – dt pressure by hardened arterial

wall Humping of vein (Salus arch) Venous banking – dt dilatation of vein prox to AV

crossing Deflection of vein as S or Z-shaped bent Turtousity of vessels – dt inc length of arterioles Attenuation of arteries – dt thickening of arterial wall

Retinopathy

Arteriosclerotic retinopathy

Retinopathy

Central serous retinopathy• Edema of macular region• More common in male• Occurs >20 y/o• Either defect in retinal pigment epith allowing

choroidal transudate to seep into retina, some form choroiditis or vascular spasm

• Principal symptoms– Blurring of central vision– Metamorphopsia, micropsia and macropsia – dt

disruption of arrangement of visual cells by edema

Retinopathy

Pigment degeneration of Retina• Charac initially by premature death of

photoreceptor cells w/ subsequent changes in pigment epith

• Transmitted as dominant, recessive or sex-linked trait

• Mc initial symptom is night blindness – dt early involvement of rods

• Field studies show ring of scotoma wc extends peripherally → loss of peripheral vision

• End stage: central vision eventually fades away

Retinopathy

Retinal detachment

• Definition: Retinal detachment refers to the separation of the neurosensory retina from the underlying retinal pigment epithelium, to which normally it is loosely attached.

Primary retinal detachment Always asso w/ breaks (usually in periphery) in retina Vitreous fluid seeps in thru retinal break and initiate separation

Retinal detachment

• Secondary retinal detachment– Dt dse process of retina, vitreous or choroid– Caused by exudates (choroiditis, Harada’s

dse); tumor cells or traction on retina

• MC symptom: photopsia• Ophthalmoscopic findigs– Elevated retina– Grayish retina– Retinal vessels appear constricted and darker

Retinoblastoma

• Definition: Retinoblastoma is a malignant tumor of early childhood that develops from immature retinal cells.

• MC intraocular tumor• Pathogenesis.

– A somatic mutation is detected in about 95% of patients. – In other patients, it is inherited as an autosomal-dominant

trait. – Changes on chromosome 13q have been observed in germ-

cell mutations• Symptoms.

– manifests itself before the age of 2 in 70% of affected children.

– Parents observe leukocoria, a whitish-yellow pupil; in 60% of these children, strabismus in 20%, and a reddened eye in 10%.

Leucocoria “cat’s eye reflex”

Retinoblastoma

• Intraocular stage: – soapy white mass in retina

• Glaucomatous stage– IOP increased– Ocular congestion and corneal edema– Vitreous filled with tumor cells

• Extraocular stage– Tumor extends out of eye into orbit via occular emissaria or thru

optic nerve• Metastasis

– Hematogenous spread to long bones– Manifests as painfull swelling of prox/distal ends

• Treatment. – Tumors <4 pupil diameters can be managed with radiation therapy

delivered by plaques of radioactive ruthenium or iodine (brachytherapy) and cryotherapy.

– Larger tumors require enucleation of the eye.

“Now, Eye’m gonna ask questions coz Eye saw you listening”

Short Quiz!

No. 110 layers of retina

(from outside to inside)

No. 2In visual blurring, if macula is involved, what

vision is affected? (Central/Peripheral)

No. 3

What retinal disease is this?

No. 4

What retinal disease is this?

No. 5What stage of hypertensive retinopathy shows areas of

hemorrhage, cotton wool spots and papilledema?

No. 6It refers to the separation of the neurosensory retina from the underlying retinal pigment epithelium, to which normally it is

loosely attached.

No. 7What do you call this condition? What disease

manifests it?

No. 8True or False:

Pulsation in retinal vein is normal.

No. 9True or False:

Disorders of the retina are painful.

No. 10What is the function of Vitamin A in the retina?

Thank you!